MAPK Cancer Research Results

MAPK, mitogen-activated protein kinase: Click to Expand ⟱
Source: CGL-CS
Type:
Mitogen-activated protein kinases (MAPKs) are a group of proteins involved in transmitting signals from the cell surface to the nucleus, playing a crucial role in various cellular processes, including growth, differentiation, and apoptosis (programmed cell death).

MAPK Pathways: The MAPK family includes several pathways, the most notable being:
1.ERK (Extracellular signal-Regulated Kinase): Often associated with cell proliferation and survival.
2.JNK (c-Jun N-terminal Kinase): Typically involved in stress responses and apoptosis.
3.p38 MAPK: Associated with inflammatory responses and apoptosis.

Inhibitors: Targeting the MAPK pathway has become a strategy in cancer therapy. For example, BRAF inhibitors (like vemurafenib) are used in treating melanoma with BRAF mutations.
Altered Expression Levels:
Overexpression: Many cancers exhibit overexpression of MAPK pathway components, such as RAS, BRAF, and MEK. This overexpression can lead to increased signaling activity, promoting cell proliferation and survival.
Downregulation: In some cases, negative regulators of the MAPK pathway (e.g., MAPK phosphatases) may be downregulated, leading to enhanced MAPK signaling.
The expression levels of MAPK pathway components can serve as biomarkers for cancer diagnosis, prognosis, and treatment response. For example, high levels of phosphorylated ERK (p-ERK) may indicate active MAPK signaling and poor prognosis in certain cancers.

Numerous reports indicate that the MAPK pathway plays a major role in tumor progression and invasion, while inhibition of MAPK signaling reduces invasion.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
2792- CHr,    Chrysin induces death of prostate cancer cells by inducing ROS and ER stress
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
DNAdam↑, TumCCA↑, MMP↓, ROS↑, lipid-P↑, ER Stress↑, UPR↑, PERK↑, eIF2α↑, GRP78/BiP↑, PI3K↓, Akt↓, p70S6↓, MAPK↑,
167- CUR,    Curcumin-induced apoptosis in PC3 prostate carcinoma cells is caspase-independent and involves cellular ceramide accumulation and damage to mitochondria
- in-vitro, Pca, PC3
MAPK↑, JNK↑, Casp3↑, Casp8↑, Casp9↑, AIF↑, GSH↓, eff↓, Apoptosis↑, DNAdam↑,
87- QC,    Quercetin inhibits prostate cancer by attenuating cell survival and inhibiting anti-apoptotic pathways
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ROS⇅, BAX↑, PUMA⇅, β-catenin/ZEB1↓, Shc↓, TAp63α↑, MAPK↑, p‑p42↑, p‑p44↑, BIM↑,
85- QC,    Quercetin inhibits invasion, migration and signalling molecules involved in cell survival and proliferation of prostate cancer cell line (PC-3)
- in-vitro, Pca, PC3
uPA↓, uPAR↓, EGFR↓, NRAS↓, Jun↓, NF-kB↓, β-catenin/ZEB1↓, p38↑, MAPK↑, cJun↓, cFos↓, Raf↓, TumCI↓, TumCMig↓,
3369- QC,    Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects
- Review, Pca, NA
FAK↓, TumCCA↑, p‑pRB↓, CDK2↑, CycB/CCNB1↓, CDK1↓, EMT↓, PI3K↓, MAPK↓, Wnt↓, ROS↑, miR-21↑, Akt↓, NF-kB↓, FasL↑, Bak↑, BAX↑, Bcl-2↓, Casp3↓, Casp9↑, P53↑, p38↑, MAPK↑, Cyt‑c↑, PARP↓, CHOP↑, ROS↓, LDH↑, GRP78/BiP↑, ERK↑, MDA↓, SOD↑, GSH↑, NRF2↑, VEGF↓, PDGF↓, EGF↓, FGF↓, TNF-α↓, TGF-β↓, VEGFR2↓, EGFR↓, FGFR1↓, mTOR↓, cMyc↓, MMPs↓, LC3B-II↑, Beclin-1↑, IL1β↓, CRP↓, IL10↓, COX2↓, IL6↓, TLR4↓, Shh↓, HER2/EBBR2↓, NOTCH↓, DR5↑, HSP70/HSPA5↓, CSCs↓, angioG↓, MMP2↓, MMP9↓, IGFBP3↑, uPA↓, uPAR↓, RAS↓, Raf↓, TSP-1↑,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   GSH↑, 1,   lipid-P↑, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   ROS↑, 2,   ROS⇅, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   EGF↓, 1,   FGFR1↓, 1,   MMP↓, 1,   p‑p42↑, 1,   Raf↓, 2,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   LDH↑, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 1,   Bak↑, 1,   BAX↑, 2,   Bcl-2↓, 1,   BIM↑, 1,   Casp3↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 2,   Cyt‑c↑, 1,   DR5↑, 1,   FasL↑, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 5,   p38↑, 2,   PUMA⇅, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   p70S6↓, 1,  

Transcription & Epigenetics ⓘ

cJun↓, 1,   miR-21↑, 1,   p‑pRB↓, 1,   Shc↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   eIF2α↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 2,   HSP70/HSPA5↓, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3B-II↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 1,   PARP↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↑, 1,   CycB/CCNB1↓, 1,   TAp63α↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

cFos↓, 1,   CSCs↓, 1,   EMT↓, 1,   ERK↑, 1,   FGF↓, 1,   IGFBP3↑, 1,   Jun↓, 1,   mTOR↓, 1,   NOTCH↓, 1,   NRAS↓, 1,   PI3K↓, 2,   RAS↓, 1,   Shh↓, 1,   Wnt↓, 1,  

Migration ⓘ

FAK↓, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   p‑p44↑, 1,   PDGF↓, 1,   TGF-β↓, 1,   TSP-1↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   uPA↓, 2,   uPAR↓, 2,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 2,   VEGF↓, 1,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CRP↓, 1,   IL10↓, 1,   IL1β↓, 1,   IL6↓, 1,   NF-kB↓, 2,   TLR4↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,  

Clinical Biomarkers ⓘ

CRP↓, 1,   EGFR↓, 2,   HER2/EBBR2↓, 1,   IL6↓, 1,   LDH↑, 1,  
Total Targets: 103

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: MAPK, mitogen-activated protein kinase
3 Quercetin
1 Chrysin
1 Curcumin
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:22  Cells:%  prod#:%  Target#:181  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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